Based on newly acquired knowledge on the mechanism of Vγ9Vδ2 T cell activation, agonistic antibodies directed against BTN3A1 and BTN2A1 (90, 91) can be used to heighten sensitivity of tumor cells to γδ T cell killing and offers a promising therapeutic strategy to enhance γδ T cell cytotoxicity. This evidence concerns the gene BTN3A1 and neoplasm.